Pyroptosis is a highly specific type of inflammatory programmed cell death that is mediated by Gasdermine (GSDM). It is characterized by inflammasome activation, caspase activation, and cell membrane pore formation. Diabetic cardiomyopathy (DCM) is one of the leading diabetic complications and is a critical cause of fatalities in chronic diabetic patients, it is defined as a clinical condition of abnormal myocardial structure and performance in diabetic patients without other cardiac risk factors, such as hypertension, significant valvular disease, etc. There are no specific drugs in treating DCM despite decades of basic and clinical investigations. Although the relationship between DCM and pyroptosis is not well established yet, current studies provided the impetus for us to clarify the significance of pyroptosis in DCM. In this review, we summarize the recent literature addressing the role of pyroptosis and the inflammasome in the development of DCM and summary the potential use of approaches targeting this pathway which may be future anti-DCM strategies.
Diabetes mellitus (DM) eventually leads to chronic vascular complications, resulting in cardiovascular diseases. DM-associated endothelial dysfunction (ED) plays an important role in the development of chronic vascular complications. Low endothelial nitric oxide synthase (eNOS) activity, inflammation, and oxidative stress all contribute to ED. The G protein–coupled receptor Takeda G protein–coupled receptor 5 (TGR5) is a membrane receptor for bile acids that plays an important role in the regulation of glucose metabolism. Recent studies have shown that TGR5 is involved in the regulation of various mediators of ED, which suggests that TGR5 may represent a target for the treatment of DM-associated ED. In this review, we summarize the principal mechanisms of DM-associated ED, then propose TGR5 as a novel therapeutic target on the basis of its mechanistic involvement, and suggest potential directions for future research.
Diabetic cardiomyopathy seriously affects quality of life and even threatens life safety of patients. The pathogenesis of diabetic cardiomyopathy is complex and multifactorial, and it is widely accepted that its mechanisms include oxidative stress, inflammation, insulin resistance, apoptosis, and autophagy. Some studies have shown that gut microbiota plays an important role in cardiovascular diseases. Gut microbiota and its metabolites can affect the development of diabetic cardiomyopathy by regulating oxidative stress, inflammation, insulin resistance, apoptosis, and autophagy. Here, the mechanisms of gut microbiota and its metabolites resulting in diabetic cardiomyopathy are reviewed. Gut microbiota may be a new therapeutic target for diabetic cardiomyopathy.
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